dc.contributor.author | EISENHART, J | |
dc.contributor.author | Akinci, Ozan | |
dc.contributor.author | KANETO, H | |
dc.contributor.author | SNYDER, C | |
dc.contributor.author | BUDINGER, GRS | |
dc.contributor.author | CHANDEL, NS | |
dc.contributor.author | LEE, VY | |
dc.contributor.author | SCHROEDL, C | |
dc.contributor.author | BRUNELLE, JK | |
dc.contributor.author | BUCCELLATO, LJ | |
dc.date.accessioned | 2021-03-03T19:15:44Z | |
dc.date.available | 2021-03-03T19:15:44Z | |
dc.date.issued | 2005 | |
dc.identifier.citation | LEE V., SCHROEDL C., BRUNELLE J., BUCCELLATO L., Akinci O., KANETO H., SNYDER C., EISENHART J., BUDINGER G., CHANDEL N., "Bleomycin induces alveolar epithelial cell death through JNK-dependent activation of the mitochondrial death pathway", AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, cilt.289, sa.4, 2005 | |
dc.identifier.issn | 1040-0605 | |
dc.identifier.other | vv_1032021 | |
dc.identifier.other | av_538dd0b3-8efe-4ee0-b835-8120b255aa35 | |
dc.identifier.uri | http://hdl.handle.net/20.500.12627/59240 | |
dc.identifier.uri | https://doi.org/10.1152/ajplung.00340.2004 | |
dc.description.abstract | Exposure to bleomycin in rodents induces lung injury and fibrosis. Alveolar epithelial cell death has been hypothesized as an initiating mechanism underlying bleomycin-induced lung injury and fibrosis. In the present study we evaluated the contribution of mitochondrial and receptor- meditated death pathways in bleomycin-induced death of mouse alveolar epithelial cells ( MLE-12 cells) and primary rat alveolar type II cells. Control MLE-12 cells and primary rat alveolar type II cells died after 48 h of exposure to bleomycin. Both MLE-12 cells and rat alveolar type II cells overexpressing Bcl-XL did not undergo cell death in response to bleomycin. Dominant negative Fas-associating protein with a death domain failed to prevent bleomycin-induced cell death in MLE-12 cells. Caspase-8 inhibitor CrmA did not prevent bleomycin-induced cell death in primary rat alveolar type II cells. Furthermore, fibroblast cells deficient in Bax and Bak, but not Bid, were resistant to bleomycin-induced cell death. To determine whether the stress kinase JNK was an upstream regulator of Bax activation, MLE-12 cells were exposed to bleomycin in the presence of an adenovirus encoding a dominant negative JNK. Bleomycin- induced Bax activation was prevented by the expression of a dominant negative JNK in MLE-12 cells. Dominant negative JNK prevented cell death in MLE-12 cells and in primary rat alveolar type II cells exposed to bleomycin. These data indicate that bleomycin induces cell death through a JNK-dependent mitochondrial death pathway in alveolar epithelial cells. | |
dc.language.iso | eng | |
dc.subject | Sağlık Bilimleri | |
dc.subject | Temel Tıp Bilimleri | |
dc.subject | Biyokimya | |
dc.subject | Fizyoloji | |
dc.subject | Dahili Tıp Bilimleri | |
dc.subject | Göğüs Hastalıkları ve Allerji | |
dc.subject | Yaşam Bilimleri | |
dc.subject | Temel Bilimler | |
dc.subject | Klinik Tıp | |
dc.subject | Klinik Tıp (MED) | |
dc.subject | Tıp | |
dc.subject | SOLUNUM SİSTEMİ | |
dc.subject | Yaşam Bilimleri (LIFE) | |
dc.subject | Biyoloji ve Biyokimya | |
dc.subject | FİZYOLOJİ | |
dc.title | Bleomycin induces alveolar epithelial cell death through JNK-dependent activation of the mitochondrial death pathway | |
dc.type | Makale | |
dc.relation.journal | AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY | |
dc.contributor.department | , , | |
dc.identifier.volume | 289 | |
dc.identifier.issue | 4 | |
dc.contributor.firstauthorID | 59946 | |